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Transcranial Doppler Ultrasonography during Head-Upright Tilt-Table Testing
- Carey S. Fredman, MD;
- Kurt M. Biermann, RN, BSN;
- Vipool Patel, MD;
- Erica L. Uppstrom, MD; and
- Arthur I. Auer, MD
- From St. John's Mercy Heart Center and Christian Northeast Hospital, St. Louis, Missouri. Acknowledgments: The authors thank Katheryne Dieckmann and Rebecca Nappier for technical assistance and Nancy La Chance for secretarial help in preparing the manuscript. Requests for Reprints: Carey S. Fredman, MD, FACC, Electrophysiology Laboratory and Pacemaker Services, St. John's Mercy Heart Center, 621 South New Ballas Road, #3005-B, St. Louis, MO 63141. Current Author Addresses: Dr. Fredman: Electrophysiology Laboratory and Pacemaker Services, St. John's Mercy Heart Center, 621 South New Ballas Road, #3005-B, St. Louis, MO 63141.
Head-upright tilt-table testing is often used to support the diagnosis of vasovagally mediated syncope [1-4]. Studies that have looked at the hemodynamic changes that occur during head-upright tilt-table testing [1] have shown that positive test results are often associated with both systemic hypotension and bradycardia and that hypotension almost always precedes bradycardia. In a minority of positive tilt-table tests, syncope results from hypotension alone.
Recently, a paradoxical increase in cerebrovascular resistance was shown to occur concomitantly with the development of hypotension and bradycardia in patients who had syncope during tilt-table testing [5]. We describe a previously unreported response in a patient who had near-syncope during tilt-table testing. The patient developed increased cerebrovascular resistance and showed a significant reduction in cerebral blood flow velocity in the absence of systemic hypotension or bradycardia.
Case Report
A 23-year-old white woman had had four episodes of syncope during an 11-day period. Some of the episodes were witnessed; all occurred shortly after the patient stood up from either a sitting or a supine position. The duration of unconsciousness was estimated to be 10 to 30 seconds. The patient did not injure herself. She stated that she became extremely warm and diaphoretic just before each syncopal episode and that her heart beat rapidly when she assumed the upright position. She had had no history of syncope before these recent episodes. Her only medications included birth control pills, and she had had no significant previous medical illness.
On physical examination, the patient's blood pressure was 104/70 mm Hg and her pulse was 88 beats/min while seated. Her blood pressure was 108/80 mm Hg and her pulse was 96 beats/min while she was standing. The results of the rest of the physical examination, the results of the cardiac examination, and the 12-lead electrocardiogram were all normal. The patient was referred for head-upright tilt-table testing.
Methods
The tilt-table test was done while the patient was fasting. Heart rate and rhythm were continuously monitored using surface electrocardiography. Blood pressure was measured with a standard sphygmomanometer while the patient was in the base-line supine position, at 1-minute intervals during the tilt-table test, and with continuous recycling during symptoms. The blood flow velocity of the middle cerebral artery was continuously monitored using a 2-MHz pulsed-wave transcranial Doppler ultrasonography system (Medasonics, Inc., Mountain View, California). The transducer was placed on the skin overlying the temporal bone above the zygomatic arch. The blood flow velocity of the middle cerebral artery was monitored at a mean depth of 50 mm from the surface of the skin. The systolic, diastolic, and peak blood flow velocities of the middle cerebral artery were measured. The mean velocity and the pulsatility index (pulsatility index = [systolic velocity − diastolic velocity]/mean velocity) were calculated. The patient was positioned upright at an angle of 80 degrees on the tilt table, and a footboard was used for weight bearing.
Results
When the patient was in the baseline supine position, her heart rate was 67 beats/min, her blood pressure was 106/59 mm Hg, mean cerebral blood flow velocity was 50 cm/s, and the pulsatility index was 0.59. Changes in blood pressure, heart rate, mean cerebral blood flow velocity, and pulsatility index are shown in Figure 1. Within 1 to 2 minutes after the tilt table was raised to the upright position, the patient became diaphoretic and began to have generalized weakness, nausea, and dizziness. Her heart rate increased to more than 140 beats/min, and her blood pressure was 100/67 mm Hg. The patient developed near-syncope and was difficult to arouse. At the peak of her symptoms and just before the tilt table was lowered to the supine position, the patient's heart rate was 139 beats/min, her blood pressure was 114/61 mm Hg, and her mean cerebral blood flow velocity was 21 cm/s. The pulsatility index had increased to 1.49. The tilt table was lowered to the supine position, and the patient's symptoms abated within 1 minute. Mean cerebral blood flow velocity and the pulsatility index returned to their baseline values.
Discussion
During tilt-table testing, we monitored blood pressure, heart rate, and heart rhythm. Additionally, we indirectly measured cerebral blood flow using the blood flow velocities of the middle cerebral artery, which were determined using transcranial Doppler ultrasonography. This technique allows noninvasive assessment of the intracranial cerebral circulation [6]. With cerebral arteriolar vasoconstriction, the pulsatility index increases, resulting in a decrease in mean cerebral blood flow velocity [7]. Although the potential limitations of transcranial Doppler ultrasonography have been described, the clinical utility of this technique has been recognized [7, 8].
Grubb and colleagues [5] recently showed that patients who had tilt-table-induced vasovagal syncope had Doppler ultrasonographic evidence of paradoxical vasoconstriction before loss of consciousness. In patients with syncope or presyncopal symptoms, mean cerebral blood flow velocity decreased by 46% and the pulsatility index increased by 295% concomitant with the development of hypotension and bradycardia. Controls had no significant alterations in cerebral blood flow patterns. Grubb and colleagues suggested that the abnormal baroreceptor responses that occurred during vasovagal syncope created a derangement in cerebral autoregulation that allowed for paradoxical vasoconstriction in the setting of increasing hypotension. They suggested that the vasoconstriction may have contributed to the syncope.
The patient we describe had symptoms that were consistent with vasovagal syncope and that were reproduced during head-upright tilt-table testing. The patient's vasovagal symptoms occurred despite the maintenance of systemic arterial pressure and in the absence of bradycardia. Using transcranial Doppler ultrasonography to measure the blood flow velocity of the middle cerebral artery, it was possible to identify a substantial decrease in the patient's mean cerebral blood flow velocity in the setting of cerebral arteriolar vasoconstriction at the time the patient became symptomatic. This case shows that disordered cerebral autoregulation may occur during tilt-table testing at the time of intense vasovagal symptoms, despite the absence of systemic vasodepression or cardioinhibition. To our knowledge, such a finding has not previously been reported, and it would suggest that the impaired cerebral autoregulation that occurs during vasovagal syncope may be manifested independently of the abnormal baroreceptor responses that usually accompany this disorder.
Fouad and coworkers [9] described a syndrome of marked orthostatic intolerance usually associated with postural sinus tachycardia and a normal blood pressure response during head-upright tilt. Blood volume determination in the patients who had this syndrome showed idiopathic hypovolemia. The authors suggested that excessive hypovolemia activated the sympathetic nervous system and, in one patient, precipitated a classic vasovagal reaction with hypotension and cardioinhibition. We did not measure blood volume in our patient, but it is possible that a similar triggering of sympathetic drive initiated that part of the vasovagal reflex leading to cerebral vasoconstriction. This occurred without the more commonly associated hypotension and bradycardia. Identifying this type of response during head-upright tilt-table testing requires the use of transcranial Doppler ultrasonography.
Dr. Uppstrom: Christian Northeast Hospital, 11125 Dunn Road, Suite 406, St. Louis, MO 63136.
Dr. Auer: St. John's Mercy Medical Center, 621 South New Ballas Road, #307-A, St. Louis, MO 63141.
Dr. Patel: University of Missouri, Division of Cardiology, 1 Hospital Drive, Columbia, MO 65212.
Mr. Biermann: St. John's Mercy Heart Center, Electrophysiology Laboratory-2L, 615 South New Ballas Road, St. Louis, MO 63141.
- Copyright ©2004 by the American College of Physicians
